Step 1 Renal

Front 1

at low, med and high doses what does dopamine do

Back 1

1) low - D1 receptor - increases kidney perfusion, (inc GFR, RBF and Na exc) also induces mesenteric vasodil
2) Med - B1 activity
3) alpha 1

Front 2

What is the path of blood through the kidney

Back 2

Ab aorta--> renal artery --> lobar --> interlobar--> arcuate --> interlobular --> afferent --> glom --> eff -> peritubular caps --> renal vein --> IVC

Front 3

Where is the JG aparatus, and where is the macula densa

Back 3

JG - aff arteriole,
MD - DCT

Front 4

Which kidney is usually taken for transplant and why?

Back 4

Left renal vein is longer

Front 5

what is the blood supply of the ureter

Back 5

Renal for the proximal 1/3, gonadal and vesicular arts

Front 6

Where does the renal artery leave the aorta at?

Back 6

L2

Front 7

What gives the BM its negative charge -

Back 7

Heparan sulfate

Front 8

What results from the loss in the charge barrier

Back 8

Nephrotic syndrome

Front 9

What is a normal GFR

Back 9

~ 100mL/min

Front 10

What is the equation for filtered load

Back 10

GFR x Px

Front 11

What is the form for exc rate

Back 11

V x Ux

Front 12

Formula for reabs rate=

Back 12

Filtered load-excretion rate

Front 13

Formula for sec

Back 13

excreted load - filtered

Front 14

At what plasma level does glucosuria begin and when are transporters fully saturated

Back 14

160-200, 350 = Tm

Front 15

What is hartnups disease

Back 15

deficiency of neutral amino acid (tryptophan) transporter, results in pellagra

Front 16

Which location reabsorbs more calcium the TAL, or the DCT?

Back 16

DCT (~15%)

Front 17

Where is the Ca/Na exhanger that is activated by PTH

Back 17

DCT

Front 18

Where are mg and ca indirectely ireabsorbed

Back 18

TAL (paracellular xport

Front 19

Which cell in the conducting tubule secretes acid

Back 19

Intercalated

Front 20

What cell responds to ADH, and what type of ADH receptor does it have

Back 20

Principal cell of the CD, V2 receptor (v1 receptor is on the vasc smooth mucscle)

Front 21

what two things does ADH respond, and which takes precedence

Back 21

Osmo and low blood volume..blood vol take precedence

Front 22

What things does aldo do

Back 22

Inc Na channels, na/kpump insertion in principal cells, enhances K and H excretion which creates a favorable na gradient for Na and H20 reabs

Front 23

what adrenergic receptor causes the release of renin

Back 23

B1

Front 24

Where is Epo released from

Back 24

Endothelial cells of the peritubular capillaries

Front 25

Where does vit D conversion occur

Back 25

prox tubule

Front 26

What are two causes of renal artery stenosis

Back 26

1) atherosclerosis
2) fibromuscular dysplasia of multiple segs (looks like a string of beads)

Front 27

How does ANP cause na loss

Back 27

It increases GFR (dil of aff constirction of eff) with no compensatory inc in na reabs

Front 28

What things cause K to shift out of a cell

Back 28

Insulin deficiency, B adrenergic antagonists (dec na/k pump), acidosis, server exercise, hyperosmolarity, digitalis, cell lysis

Front 29

What causes K to shift into a cell

Back 29

Insulin, B agonists alkalosis, hypoosmo

Front 30

What are the causes of anion gap acidosis

Back 30

MUD PILES
Methanol
Uremia
Diabetic Ketoacidosis
Paraldhyde or phenformin
Iron tablets or INH
Lactic Acidosis
Ethlene Glycol
Salicylates (after some hours because at first they cause hypervent --> resp alkalosis so you see a progression from that to mixed to acidosis)

Front 31

What are the causes of nonanion gap acidosis

Back 31

Diarrhea
Glue Sniffing
Renal Tubular Acidosis
Hyperchloremia
Saline administration (gain of cl)

Front 32

What is the mechanism of contraction alkalosis with diuretics

Back 32

Renal loss of Na is followed by Cl reabsorption of HCO3 follows to maintain neutrality, volume also decreases so some aldo is released which causes H wasting.

Front 33

What causes metabolic alkalosis?

Back 33

Diuretic use, Vomiting, antacid use, and hyperaldosteronism (H wasting)

Front 34

Why does uremia cause acidosis

Back 34

Decreased excretion of H+ as NH4, de excretion of sulfate, phosphate,urate, hippurate, hence anion gap,

Front 35

What causes Type 1, Type 2, or type 4 acidosis

Back 35

Type 1 - defect in CT ability to excrete H+ associated with hypokalemia and risk for ca containing Kidney stones. (Urine ph >5.5)
Type 2 - defect in prox tubule HCO3 reabsorption. Assoc with hypokalemia and hypophosphatemic rickets (urine pH less than 5.5)
Type4 - Hypoaldosteronism or lack of collecting tubule response to aldosterone. Assoc with hyperkalemia nad inhibition of ammonium excretion in the prox tubule. Leadds to dec urine pH due to dec buffering capacity
****All are non anion gap

Front 36

What is associated with RBC casts

Back 36

Glomerulonephritis, ischemia, or malignant hypertension.

Front 37

What is associated with granular ('muddy') casts

Back 37

Acute tubular necrosis

Front 38

What nephritic syndrome has the following picture:
LM - enlarged hypercellular, neutrophils, lumpy bumpy appearnace
EM - subepithelial immune complex humps
IF- granular

Back 38

Acute post strep glomerulonephritis
See in kids...see peripheral and periorbital edema. Resolves spontaneously.
Low C3 norm c4, No IgAdeposits, IgG complexes. See 1-2 w after infection (unlike bergers)

Front 39

What Nephritic condition has the following characteristics:
LM and IF- Cresent moon shape.

Back 39

There are a lot of different types of this some causes are goodpasutres, wegners and microscopic polyangitis

****The cresent consists of fibrin and plamsa proteins (C3b) with glomerular parietal cells, monoctyes and macrophages --> rupture in gbm allows infiltrates into bowmans space. Allows fibrinogen to leak --> fibring --> compression/collapse of the glom

Front 40

What are the three main types of RPGN

Back 40

1-goodpasture - type II hypersensitivity abs (igG and c3) to GB and alveolar BM = LINEAR IF
2- Wegners - no IF CANCA
3- microscopic polyangiitis - no IF see PANCA
4- Pauci immune - nothing

** lupus and lots of other things can cause this

Front 41

What Nephritic condition has the following characteristics
LM - wire looping of the caps
EM - subedonthelial DNA-antiDNA ICs
IF - granular

Back 41

Diffuse proliferative glomerulonephritis - due to SLE or MPGN - most common cause of death in SLE. SLE and MPGN can present as nephritic and nephrotic

Front 42

What Nephritic condition has the following characteristics:
LM and IF - IC deposit in the mesangium, increased synthesis of IgA

Back 42

Bergers (IgA nephropathy), Often presents/flares with a URI or acute gastroenteritis
** if this presents with extrarenal sx = HSP

Front 43

What Nephritic condition has the following characteristics: Split BM and mutations in type IV collagen

Back 43

Alports - see nerve disorders, ocular disorders, deafness, X linked or AR (variable)

Front 44

What Nephrotic condition has the following characteristics:
LM- diffuse capillary and GBM thickening
EM- 'spike and dome' appearnace with subepi depositis
IF - granular SLEs nephrotic presentation IgG and/or C3

Back 44

Membranous glomerulonephritis see little hairs on silver stain,

Caused by drug, infections SLE, solid tummors
ICs deposit in GBM complements are activated = damage

Front 45

What Nephrotic condition has the following characteristics:
LM Normal Glom
Em foot process effacement

Back 45

Minimal change dz,,,May be triggered by a recent infection of an immune stimulus. Most common in kids. Responds to CORTICOSTEROIDS. Selective loss of albumin NOT globulins due to GBM polyanion loss

Front 46

What do you see in amyloidosis nephrotic

Back 46

LM - congo red stain, apple green birefriengence, subendo and mesangial deposits
* assoc with multple myeloma, TB, RA

Front 47

Whats the nephrotic disorder:
LM - mesangial expansion, GBM thickening, nodular glomerulosclerosis (kimmelstiel wilson lesion)

Back 47

Diabetic glomerulonephropathy -
GBM - secondary to Nonenzymatic glycosylation of the GBM, see the mesangial expansion due to NEG of effert arts (constriction) that increases the GFR.

Front 48

What Nephrotic condition has the following characteristics:
segmental sclerosis and hyalinosis

Back 48

FSGS - most common in adults, very common in HIV,

Front 49

What Nephrotic condition has the following characteristics: Tram track appearnce due to GBM splitting by mesangial ingrowth.

Back 49

MPGN
TII - EM dense deposits
Can have a nephrotic component

Front 50

What is type I MPGN assoc with

Back 50

HBV, HCV, or cryoglobinemia, sub endo ICs with granular IF, AI dz (SLE, SS)alpha anti trypsin, CLL

Front 51

Type II mpgn

Back 51

associated with the C3 nephritic factor that binds to c3 convertase causing sustained activation of C3 resulting in very low c3 levels. Diffuse intramembranous deposis, hypertension. Majority have hematuria. Majority progress to CRF

Front 52

What can cause Oxalate crystals?

Back 52

Ethylene glycol or Vitamin C abuse

Front 53

What stone is radiolucent

Back 53

Uric acid stones. Has a strong assoc with hyper urecemia.

Front 54

What stone can you treat with Acetazolamide

Back 54

Cystine

Front 55

What stone is associated with staghorn infection

Back 55

Stuvide (ammonium magnesium phosphate

Front 56

What organisms are involved in stuvite stone formation

Back 56

Proteus, klebs, staph (urease positive

Front 57

RCC - what do you see

Back 57

Polygonal clear cells. Most common in men 50-70 yo. Inc incidence with smoking and obesity

Front 58

What are the signs and sx of RCC

Back 58

Hematuria, palpable mass, secondary polycythemia, flank pain, fever and weight loss. Assoc wit hparaneoplastic syndromes (epo,acth, pthrp and prolactin.) Invades the IVC and spreads hematogenously, mets to lung and bone.
* assoc with VHL
RF - cadmium exp

Front 59

AWhat is a onchocytoma

Back 59

A proximal tubule CD tumor brownish due to lost of mito

Front 60

What do you see, what are the s/sx and whats the gene assoc with Wilms tumore

Back 60

kids tumor, ages 2-4, contains embryonic glomerular structures. Presents with huge palpable flank mass and/or hematuria.
* Due to a deletion on chromosome 11p of the WT1 gene

Front 61

What is WAGR complex

Back 61

Wilms tumor, aniridia, Genitourinary malformation and mental-motor retardation

Front 62

What is a consequence of a angiomyolipoma

Back 62

retroperitoneal hemorrhage

Front 63

Transitional cell carc s/sx RFs

Back 63

This is the most common tumor of the urinary tract
S/sx - painless hematuria (always consider bladder cancer) can occur in the renal calyces, pelvis ueter and bladder

RFs - phenactein, smoking, aniline dye, cyclophosphamide

Front 64

what infection affects the cortex with relative sparing of the glom/vessels,...See PMN infiltration it present wit hfever, CVA tenderness N/V... (BE SPECIFIC)

Back 64

Acute pyelo
Ascending - E coli
Hematogenous spread - tb and Staph

Front 65

What infection causes coarse, asymmetric corticomedullary scaring with blunted calyces. You can see tubules with eosinophilic casts and lymphocyte infiltration(aka as thyroidization of the kidney)

Back 65

Chronic Pyelo, RF: Dm, vesicuouteral reflux, obstructive = hydronephrosis --> dilation of the calyces

Front 66

What causes fever, maculopapular rash, oliguria, azotemia, pyuria (usually eosinophilic),

Back 66

Drug induced interstitial nephritis drugs like PCN, Sulfonamides, rifampin, diuretics, can act as haptens inducing hypersensitivity...this occurs 1-2 weeks after drug anmiistration

Front 67

What happens in diffuse cotrical necrosis

Back 67

Acute generalized cortical infarction of BOTH kidneys. Likely due to a combo of vasospasm and DIC, rapidly fatal if extensive. Assoc w/ obstetric catastrophes like abruptio placentae and septic shock.

Front 68

What are the causes of acute tubular necrosis and the key finding

Back 68

Most common cause of ARF in hospital but self reversible. Fatal if left untreated. Associated with renal ischemia (shock and sepsis), crush injury (myoglobinuria) and toxins ...
** Granular casts are the key finding aka muddy brown

Front 69

What are the three phases of ATN and the main findings

Back 69

1) Inciting even (~36hrs)
2) Maintenance - low urine output, hyper K, anion gap met acidosis,
3) reovery - brisk diuresis, hypokalemia (2-3w)
See a sloughing off of epi cells and a flattening of the brushborder

Front 70

what 2 places does ischemic damage mostly affect

Back 70

PCT and TAL due to high ATP demand

Front 71

What is renal papillary necrosis associatedwith and what is the pathology

Back 71

Assoc w/ 1. DM 2. Acute pyelo 3. Chronic phenacetin use 4. Sickle cell....The papillae slough off --> gross hematuria, proteinuria, may be triggered by a recent infection or immune stimulus.

Front 72

What is amnion nodosum -

Back 72

In oligohydramnios (potters) the fetuses skin touches the amnions --> squamous cell nodules on the placental surface form.

Front 73

What genetic condition is associated with horseshoe kidney

Back 73

Turners

Front 74

what are some other congenital renal abnormalities

Back 74

An ectopic kidney (usually in the pelvis) or a dupicate ureter

Front 75

What are the ecg signs of hyperkalemia

Back 75

Peaked Ts, St depressions, prolonged PR, wide QRS, may get heart block

Front 76

What are the ecg signs of hypokalemia

Back 76

Flattening or T inversions, U waves, St depression, premature contractions arrythmias

Front 77

What are the lab values for urine osm, urine na, BUN/Cr, and fena for prerenal failure

Back 77

Urine osm >500
Urine Na <10
Fena<1%
Serum BUN/Cr: >20
**Prerenal is due to ischemia/dec in GFr

Front 78

For renal azotemia what are the:
Urine osm
Urine Na
Fe na
Serum BUN/Cr

Back 78

Urine osm <350
Urine Na >20
Fe na >2%
Serum BUN/Cr <15
** Generally due to acute tubular necrosis or ischemia/toxins, less commonly due to actue glomerulonephritsi (RPGN)

Front 79

For post renal azotemia what are the:
Urine osm
Urine Na
Fe na
Serum BUN/Cr

Back 79

Urine osm <350
Urine Na >40
Fe na >4%
Serum BUN/Cr >15 (15-20)
** usually due to outflow obstruction (stones, BPH, neoplasia, congen anomalies. only occurs with BILATERAL obstruction

Front 80

What do you always see in prerenal failure

Back 80

Oliguria

* can also have hypovol, hypo tension low CO, ypoalbumin, inc reas reabs, inc RAS, ADH

Front 81

What are some high yield consequences of Chronic Renal Failure

Back 81

- Na/H2o retention (CHF, pulm edema, HTN)
-Hyperkalemia
-Uremia (marked by inc BUN and inc creatinine) --> nausea, anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction
-anemia
-renal osteodystrophy (ca wasting and phosphate retention, secondary hyperparathyroidism)
- Dyslipidemia (esp Inc in trigylcerides)
-Growth retardation and development delay in kids
-hypermagnesemia

Front 82

How does ADPKD present, gene? assoc w/?

Back 82

Flank pain, hematuria, HTN, UTI, progressive renal failure, gene is APKD1 or APKD 2 (pkd1 encodes a prto that inc cohesiveness bn tubular cells so over time you have inc breakdown)
** assoc w/ MVP, polycystic liver dz and berry aneurysms, colonic diverticula?

Front 83

ARPKD

Back 83

Infantile presentation, AR
- Assoc with congen hepatic fibrosis, signif renal failure in utero can lead to potters, concerns for the future are hypertension, portal HTN, and progressive renal insufficiency

Front 84

What do you see histologically or grossly in ARPKD

Back 84

Small radiating cysts that originate from any part of the kidney

Front 85

What do youy see histologically in ADPKD

Back 85

Cysts arise from the tubular structures

Front 86

What are dialysis cysts?

Back 86

Cortical and medullary cyts that result from long standing dialysis

Front 87

What are simple cysts

Back 87

Benign common incidental, thin, nonenhancing, cortical, fluid filled

Front 88

What is medullary cystic disease

Back 88

Medullary cysts that can sometimes lead to fibrosis and progressive renal insufficiency with urinary concentrating defects. U/s shows small kidney. Poor prog

Front 89

What is medullary sponge kidney

Back 89

Common, benign cystic dilations of the medullary collecting ducts. CORTEX IS USUALLY SPARED. Usually an incdiental finding, asymptomatic but sometimes dfferent than med cystic dz.

Front 90

What features are common to MPGN I and II

Back 90

Both have nephritic and nephrotic components with slow progression to renal failure,
- They both have large glm and hypercellular prolif of mesangial cells, neothelial cell and inc matrix
- they both have mesangial ingrowth and new GBM --> thick GBM with a tramtrack or double contour appearance

Front 91

What are the subendothelial deposits made of in MPGN I, what are the serum abnormalities

Back 91

C3, IgG, C1 and C4(activates classic and alternative paths)
_ Dec serum c1,c4,c3

Front 92

What are the intramembranous deposits in MPGN II

Back 92

C3 and IgGonly
zzzserum - dec C3 activate only alternative pathway, see C3 nephritic factor

Front 93

what are some causes in of nephrotoxic ATN

Back 93

most common - aminoglycosides, lead, mercury, radiographic contrast, GN sepsis, myogloinuria 2 to trauma or crush injury, direct injection into PCT gentamicin, ethylene glycol(massive intratubular oxalate crystal deposits that polarize light

Front 94

what three mechanisms lead to alkalosis in loop diuretics and HCTZ

Back 94

1) volume contraction --> inc ATII --> Inc Na/H excharger --> inc serum HCO3
2) K loss leads to K exiting cells (via H/K exchanger)
3) In low K state H rather than K is exchanged for Na in the cortical collecting tubule leading to alkalosis and paradoxical aciduria

Front 95

How do loop diuretics inc Ca sec

Back 95

Abolish lumen positive potential in the thick ascheding limb, Dec paracellular Ca --> hypocalcemia inc urine ca

Front 96

How do thiazides inc ca abso

Back 96

Volume dep --> inc Na reabs (via reflex w/ adh) --> enchances paracellular ca reabs in LOH, thiazides also block luminal Na/Cl cotransport in the DCT --> inc Na gradient --> inc intersititial Na/Ca exchange --> hypercalc

Front 97

WHere does acute pyelonephritis hit and spare

Back 97

affects the cortex, relative sparing of glom and vessels

Front 98

In what condition do you see eos in the interstitum with azotemia

Back 98

Drug induced interstitial nephritis

Front 99

What do you see pericarditis in

Back 99

Renal failure